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Pharmacology Flashcards

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1
Q

What is medicine optimisation?

A

looks at the value which medicines deliver, making sure they are clinically-effective and cost-effective

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2
Q

What does medicine optimisation help patients do?

A

Improve their outcomes
Take their medicines correctly
Avoid taking unnecessary medicines
Improve medicines safety
Reduce wastage of medicines

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3
Q

What are some examples of medicine non-adherance?

A

Not taking prescribed medication
Taking bigger/smaller doses than prescribed
Taking medication more/less often than prescribed
Stopping the medicine without finishing the course
Modifying treatment to accommodate other activities(work, social)
Continuing with behaviours against medical advice(diet, alcohol, smoking)

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4
Q

Unintentional examples of medicine non-adherance

A

Difficulty understanding instructions
Poor dexterity
Inability to pay
Forgetting

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5
Q

Intentional examples of medicine non-adherance

A

Patients’ beliefs about their health/condition
Beliefs about treatments
Personal preferences

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6
Q

What is adherance?

A

the degree to which a patient correctly follows medical advice

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7
Q

What are the impacts of good doctor-patient communication?

A

Better health outcomes.
Higher adherence to therapeutic regimens in patients.
Higher patient and clinician satisfaction.
Decrease in malpractice risk.

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8
Q

What is pharmacokinetics?

A

The fate of a chemical substance administered to a living organism

What the body does to the drug

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9
Q

What is pharmacodynamics?

A

The biochemical, physiological and molecular effects of a drug on the body

What the drug does to the body

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10
Q

What 12 ways can drugs be administered?

A

IV (intravenous)
IA (intra-arterial)
IM (intramuscular)
SC (subcutaneous)
PO (oral)
SL (sublingual)
INH (inhaled)
PR (rectal)
PV (vaginal)
TOP (topical)
TD (transdermal)
IT (intrathecal)

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11
Q

Which 2 ways of administering a drug ensure 100% of dose reach systemic circulation?

A

Intravenous
Intraarterial

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12
Q

How can drugs permeate across membranes?

A

Passive diffusion through hydrophobic membrane
Passive diffusion through aqueous pores
Carrier mediated transport

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13
Q

What factors can affect drug absorption?

A

Lipid solubility (affecting diffusion)
Drug ionisation (ionised drugs have poor lipid solubility and are poorly absorbed)

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14
Q

What factors affect oral drug absorption?

stomach

A

Drug ionisation
Low pH in stomach might degrade molecule
Gastric enzymes might digest
Full stomach will slow absorption
Gastric motility
Previous surgery

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15
Q

Where are weak acids and bases best absorbed?

A

Weak acids: best absorbed in the stomach
Weak bases: best absorbed in the intestine

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16
Q

What factors affect oral drug absorption?

Intestine

A

Drug structure (large or hydrophilic molecules are poorly absorbed)
Medicine formulation (coating can control time between administration and drug release)
P-glycoprotein (substrates are removed from intestinal endothelial cells back into lumen)

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17
Q

What is first pass metabolism?

A

Metabolism of drugs preventing them reaching systemic circulation

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18
Q

What happens in first pass metabolism?

A

Degradation by enzymes in intestinal wall
Absorption from intestine into hepatic portal vein and metabolism via liver enzymes

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19
Q

What is bioavailability?

A

proportion of administered dose that reaches the systemic circulation

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20
Q

How can you avoid first pass metabolism?

A

giving via routes that avoid sphlanchnic circulation (eg rectal)

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21
Q

What is bioavailability dependent on?

A

Dependent on extent of drug absorption and extent of first pass metabolism

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22
Q

Pros and cons of rectal administration

A

Pros: Local administration
Avoids first pass metabolism
Nausea and vomiting

Cons: Absorption can be variable
Patient preference

e.g. diazepam in epileptic seizure

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23
Q

Pros and cons of inhaled administration

A

Pros: Well perfused large surface area
Local administration
Cons: inhaler techniques can limit effectiveness

e.g. salbutamol for asthma

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24
Q

Pros and cons of subcut administration

A

Pros: Faster onset than oral
Formulation can be changed to control rate of absorption

Cons: not as fast as IV

e.g. long lasting insulin

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25
What affects drug distribution?
Molecule size (smaller distributes easier) Lipid solubility Protein binding (if drug molecule bound to albumin it can't do its action or permeate across barriers)
26
Pros and cons of transdermal administration
Pros: Provides continuous drug release Avoids first pass metabolism Cons: Only suitable for lipid soluble drugs Slow onset of action | e.g. fentanyl patches for chronic pain
27
What is the volume of distribution?
Volume of plasma required to contain the total administered dose | Theoretical volume a drug will be distributed in the body
28
Link between volume of distribution and drug distribution
Drugs that are well distributed will have high Vd Drugs that are poorly distributed will have low Vd
29
How can drugs reach the CNS?
High lipid solubility. e.g. psychiatric drugs usually very lipid soluble (therefore large Vd) Intrathecal administration to bypass blood brain barrier (e.g. baclofen in MS and spinal cord injury, chemotherapy) Inflammation of BBB (causes barrier to become leaky) so drugs thata can't normally permeate it can
30
Things to consider when prescribing: distribution
Changes in distribution caused by disease states (e.g. sepsis increases leakyness and increases distribution) Age related changes leads to smaller volume of distribution Drugs able to cross BBB more likely to cause CNS side-effects Caution dosing drugs with a small Vd using actual body weight in obese patients
31
What is drug elimination?
the process by which the drug becomes no longer available to exert its effect on the body
32
What is drug metabolism?
modification of chemical structure to form new chemical structure
33
What are the 2 phases of drug metabolism?
Phase 1: Oxidation/reduction/hydrolysis to introduce reactive group to chemical structure Phase 2: Conjugation of functional group to produce hydrophilic, inert molecule
34
What happens in phase 1 drug metabolism?
Cytochrome P450 (CYP450) enzymes are responsible for majority of phase 1 metabolism Located mostly in the liver (extrahepatic: small intestine, lung) Lipophillic, unbound drug molecules will readily cross hepatocyte membrane Produces a reactive metabolite by creating or unmasking a reactive functional group | introduce reactive group to chemical structure
35
How can CYP enzyme function vary?
Genetic variation Reduced function in severe liver disease Interactions enzyme inhibiting/inducing drugs or food can reduce/increase enzyme activity
36
What happens in phase 2 drug metabolism?
Conjugation of an endogenous functional group (glycine, sulfate, glucuronic acid) to produce a non-reactive polar (therefore hydrophilic) molecule Hydrophyllic metabolite can then be renally excreted
37
Things to consider when prescribing: metabolism
In severe liver impairment may need reduced dose/frequency, additional monitoring or avoidance CYP450 enzyme induction/inhibition drug interactions (to be discussed in detail in Drug Interactions lecture) Saturation of metabolic pathways can lead to accumulation/toxicity of drug and or metabolites
38
How can drugs and metabolites be excreted?
Liquids (small, polar molecules): urine, bile, sweat, tears, breast milk Solids (large molecules): faeces (through biliary excretion) Gases (volatiles): expired air
39
How does renal excretion work?
Glomerular filtration Active tubular secretion: drug molecules transported from blood into tubule by carrier systems (OAT, OCT) Passive reabsorption: diffusion down the concentration | OAT: organic anion transporter OCT: organic cation transporter
40
Things to consider when prescribing: drug elimination/excretion
Kidneys excrete drugs and drug metabolites (active and inactive) Reduced kidney function can lead to accumulation and toxicity of renally cleared drugs
41
What are the 4 pharmacokinetic processes?
Absorption Distribution Metabolism Excretion
42
What happens in first order kinetics?
Rate of elimination is proportional to the plasma drug concentration (processes involved in elimination do not become saturated) A constant % of the plasma drug is eliminated over a unit of time
43
What happens in zero order kinetics?
Rate of elimination is NOT proportional to the plasma drug concentration (metabolism processes become saturated) A constant amount of the plasma drug is eliminated over a unit of time
44
What is the half life of a drug dependent on?
Dependent on clearance (CL) of drug from body by all eliminating organs (hepatic, renal, faeces, breath) Dependent of volume of distribution (Vd) - A drug with large Vd will be cleared more slowly than a drug with a small Vd
45
What is drug half life not dependent on?
not dependent on drug dose or drug formulation
46
When is a drug cleared from the body?
A drug will be 97% cleared from the body after 5 x half lives (considered ‘cleared’ in clinical practice)
47
What is the relevance of drug half life in clinical practice?
* Drug dosing (short t1/2 will need more frequent dosing) * Organ dysfunction (t1/2 may be increased) * Adverse drug reactions or management of toxicity (how long will drug take to be removed and symptoms to resolve) * Short t1/2 increases risk of discontinuation/withdrawal symptoms (such drugs may need dose weaning on cessation)
48
What is drug steady state?
rate of drug input is equal to rate of drug elimination
49
What is Css and the time to Css?
Css = drug plasma concentration at steady state Time to Css = 5 x t1/2 (after treatment initiation and after a dose increase)
50
How can you reduce time to reach steady state?
Give a loading dose
51
When would continuous IV infusion be used?
Critical care patients Antibiotics Unfractionated heparin General anaesthetics
52
What drugs require a loading dose?
Digoxin Vancomycin Teicoplanin Amiodarone Heparin
53
Where should the steady state lie?
Aim for Css which lies between the Maximum safe concentration (MSC) and minimum effective concentration (MEC)
54
What drugs follow zero order kinetics?
ethanol phenytoin
55
What does drug clearance (CL) mean?
rate of drug elimination by all eliminating organs
56
What does half-life (t1/2) mean?
time taken for plasma drug concentration to fall 50%
57
What does a narrow therapeutic window mean?
Drugs with a narrow window between minimum effective concentration and maximum safe concentration
58
Examples of drugs with a narrow therapeutic window
vancomycin gentamicin phenytoin digoxin theophylline lithium
59
What does pharmacogenomics mean?
The use of genetic and genomic information to tailor pharmaceutical treatment to an individual
60
Benefits of pharmacogenomics
Improved patient outcomes Cost efficiency
61
How can genomics affect medicines use? | pharmacokinetics
variations in drug metabolism (eg CYP450 enzymes) - variations in efficacy - increased incidence in adverse drug reactions
62
How can genomics affect medicines use? | pharamcodynamics
variations in drug receptor - variations in efficacy (‘on’ targets) - increased incidence of adverse drug reactions (ADRs) (‘on’ and ‘off’ targets)
63
What is a receptor?
A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects | ligand can be exogenous or endogenous (e.g. drugs or hormones)
64
What are the different types of receptors?
Ligand-gated ion channels G protein coupled receptors Kinase-linked receptors Cytosolic/nuclear receptors
65
What do Kinase-linked receptors do?
Kinases catalyze the transfer of phosphate groups between proteins Phosphorylation
65
How do G protein coupled receptors work?
Largest and most diverse group of membrane receptors in eukaryotes Activated by peptides, lipids, sugars Activity is regulated by ability to bind and hydrolyze GTP to GDP
65
How do nuclear receptors work?
Modify gene transcription
66
What is an agonist?
a compound that binds to a receptor and activates it
67
What is an antagonist?
a compound that reduces the effect of an agonist | prevents receptor activation by agonists
68
Examples of endogenous ligands
Neurotransmitters Hormones
69
Example of an exogenous ligands
drugs
70
What is an enzyme inhibitor?
a molecule that binds to an enzyme and (normally) decreases its activity
71
How does an enzyme inhibitor work?
prevents the substrate from entering the enzyme's active site and prevents it from catalyzing its reaction
72
What are the 2 types of enzyme inhibitors?
Irreversible inhibitor: usually reacts with enzyme and changes it chemically Reversible inhibitor: binds non-covalently and different types of inhibition are produced depending on what it binds to
73
How do statins work?
Block the rate limiting step in the cholesterol pathway HMG-CoA reductase inhibitors
74
Why are statins used?
primary prevention of cardiovascular disease lipid lowering (reduce cholesterol levels)
75
What doe ACE inhibitors do?
Inhibiting ACE reduces ATII production and therefore causes a reduction in blood pressure
76
What are the naturally occuring opioids?
Morphine Codeine (weak)
77
What are the synthetic opioids?
Fentanyl Pethidine Alfentanil Remifentanil
78
Example of an opioid agonist
Naloxone
79
What is the difference between injecting opioids and giving them orally?
50% bioavailability orally 10mg orally = 5mg IV/IM/SC
80
What are the side effects of opioids?
Respiratory depression Sedation Nausea and vomiting Constipation Itching Immune supression
81
What receptors are in the sympathetic nervous system?
Alpha 1 and 2 Beta 1 and 2
82
What is affinity?
How strongly a drug binds to a receptor
83
What is potency?
amount of medication needed to elicit an effect
84
What's the link between potency and affinity?
higher affinity = higher potency higher affinity = effect at a lower dose
85
What is intrinsic activity?
ability of a drug-receptor complex to produce a maximum functional response
86
What is efficacy?
maximum response that can be achieved with a drug
87
What are competive antagonists? ## Footnote example
meds reversibly bind to same receptor site as the agonist but doesn't activate it binds and dissociates quickly inhibition when more ligands are present decreases potency but not efficacy ## Footnote beta-blockers
88
What are non-competitive antagonists? ## Footnote example
bind to allosteric sites not to the same as agonist's site alters receptor shape so unrecognisable for ligand irreversible or slow dissociation receptor won't activate despite how many agonists present | decreases efficacy ## Footnote botox affecting ACh receptors
89
Difference between competitive and non-competitive antagonists
Comp affect agonist potency Non-comp affect agonist efficacy Comp bind and dissociate quickly Non-comp are irreversible or dissociate slowly
90
What is inverse agonism?
When a drug that binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist
91
Example of a selective and non-selective agonist
Salbutamol is a b2-adrenoceptor agonist (selective for beta 2) Isoprenaline is a b-adrenoceptor agonist (non-selective for all beta)
92
What is an adverse drug reaction?
noxious and unintended response to medicinal product
93
What are the impacts of an adverse drug reaction on patients?
- Reduced QoL - Poor compliance - Reduced confidence in clinicians and the healthcare system - Unnecessary investigations or treatments
94
What is the impact of adverse drug reactions on the NHS?
- Increased hospital admissions - Longer hospital stays - GP appointments - Inefficient use of medication
95
What are the different types of ADRs? | (ABCDEFG)
Augmented Bizarre Chronic Delayed End of use Failure of treatment Genetic
96
What is an augmented ADR? ## Footnote example
exagerrated effect of a drug at therapeutic dose ## Footnote respiratory depression in opiates
97
What is a bizarre ADR? ## Footnote example
not related to pharmacology of the drug or the dose ## Footnote anaphylaxis
98
What is an end of use/withdrawal ADR? ## Footnote example
ADR after stopping drug ## Footnote e.g. rebound tachycardia after stopping beta blockers
99
What is a chronic ADR? ## Footnote example
Continue after drug has been stopped ## Footnote osteonecrosis of the jaw with bisphosphonates
100
What is a failure of treatment AR? ## Footnote example
unexpected treatment failure ## Footnote drug-food or drug-drug interaction
101
What is a genetic ADR? ## Footnote example
drug irreversibly damages genome ## Footnote thalidomide
102
What is specificity of a drug?
the extent to which a drug produces only the desired therapeutic effect without causing any other physiological changes ## Footnote High specificity less side effects
103
What is drug selectivity?
a drug's strong preference for its intended target over other targets
104
How can ADRs be classified? ## Footnote not A-G
Dose-related - hypersusceptibility: ADRs at subtherapeutic doses (e.g. anaphylaxis with penicillin) - collateral: at intended dose - toxic effects: supratherapeutic (paracetamol overdose) Time dependent Susceptibility
105
Who is at an increased risk of ADRs?
Atopic individuals- greater risk of immune mediated ADRS Children and neonates- limited data, weight based dosing Reduced drug clearance due to organ dysfunction Extremes of weight- does adjustments may be needed to avoid under/over dosing Females Polypharmacy Advanced age Genetic variants- CYP450 altered metabolism
106
How are ADRs detected?
Pre-clinical testing Clinical trial data Post-marketing surveillance Pharmacovigilance (overseen by MHRA, yellow card scheme)
107
When did the yellow card scheme start and what are the strengths?
1963 Confidential No fear of litigation Quick Accessible
108
What are the weaknesses of the yellow card scheme?
Underreporting: only 5% of ADRs Relies on HCPs recognising ADRs Doesn't indicate incidence
109
What changes can be made when an ADR is confirmed?
Adding ADR info to product (BNF) Restrictions in use Changes in legal classification Increased monitoring Withdrawal from market
110
What is the definition of pain?
An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage
111
What are the steps of the WHO analgesic ladder?
1: NSAID or paracetamol 2: weak opiods (codeine, tramadol) 3: strong opiods (morphine, fentanyl, oxycodone)
112
What are the main side effects of NSAIDs?
Gastritis with dyspepsia (indigestion) Stomach ulcers Exacerbation of asthma Hypertension Renal impairment Coronary artery disease, heart failure and strokes (rarely)
113
When might NSAIDs be inappropriate?
Asthma Renal impairment Heart disease Uncontrolled hypertension Stomach ulcers
114
What is commonly prescribed with an NSAID?
PPI
115
What are the side effects of opioids?
Constipation Skin itching (pruritus) Nausea Altered mental state (sedation, cognitive impairment or confusion) Respiratory depression (usually only with larger doses in opioid-naive patients)
116

Phase 2a (14 decks)

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